ReviewDiscover oncology2026
Insulin resistance as a modifiable contributor to breast cancer: mechanisms, biomarkers, and therapeutic implications.
Review in Discover oncology, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
2 citing papers in PubMed.
- NUPR1 in breast cancer: mechanisms and potential applications.Frontiers in physiology · 2026Review
- Sarcopenia in breast cancer: prognostic values and emerging therapeutic strategies.Frontiers in surgery · 2026Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
3 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Insulin resistance (IR) has emerged as a metabolically relevant contributor to the development and progression of breast cancer (BC), with a case fatality of nearly 15%. IR mainly shows a relationship with obesity, type 2 diabetes mellitus (T2DM), and persistent low-intensity inflammation, and promotes a pro-tumorigenic environment through hyperinsulinemia, enhanced signaling through insulin, along with insulin-like growth factor (IGF), adipocytokine imbalance, and metabolic reprogramming. IR activates mitogenic phosphatidylinositol 3-kinase (PI3K)-protein kinase B (AKT) and mitogen-activated protein kinase (MAPK) routes, increases estrogen bioavailability, and supports survival of tumor cells alongside resistance to therapeutic interventions. IR markers, such as the triglyceride-glucose index (TyG) and homeostatic model assessment of insulin resistance (HOMA-IR), have been linked to higher BC risk, aggressive tumor phenotypes, and adverse clinical outcomes. Ongoing studies also show that IR-related adipocytokines, such as adipsin and visfatin, interact with metabolic dysfunction to increase BC risk independent of obesity (OR = 18.5, 95% CI: 2–159.5 and OR = 11.25, 95% CI: 1.3–98, respectively). With the accessibility of IR indices, their integration into BC risk stratification, prognostic assessment, and treatment planning offers a promising path for precision oncology. This review synthesizes preclinical, epidemiological, and clinical evidence to examine the mechanistic links between IR and BC and also highlights translational opportunities for prevention, prognosis prediction, and therapeutic opportunities in breast tumorigenesis, useful for both physicians and researchers. Current evidence appears supportive of a relationship between IR and BC development, progression, and treatment outcomes. However, the extent of this relationship and its clinical utility still needs further investigation. The inclusion of IR-linked parameters as indicators for BC risk assessment and prognosis may help identify patients who are likely to benefit from metabolic interventions.
Identifiers
What OpenQuestion holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.